By way of definition, in the field of automatic implantable arrhythmia control devices, the term "cardioversion" or "cardioverter" refers to the process of and device for discharging relatively high energy electrical shocks or pulses into or across cardiac tissue to arrest a life threatening tachyarrhythmia. Cardioversion shocks or pulses may or may not be synchronized with a cardiac depolarization or rhythm and may be applied to arrest a malignant ventricular tachycardia or ventricular fibrillation with a selectable or programmable pulse energy. The arrest of atrial or ventricular fibrillation by such pulses is referred to as "defibrillation" (a form of cardioversion), and "defibrillators" have been characterized as a form of cardioverter. Products have been described and sold as combined, multiprogrammable, "pacemaker/cardioverter/defibrillator" systems for providing programmable staged therapies of anti-tachyarrhythmia pacing, synchronized cardioversion pulses and unsynchronized defibrillation pulses. In the following description and claims, it is to be assumed that the terms "cardioversion" and "defibrillation" are interchangeable, and that use of one term is inclusive of the other device or operation, unless specific distinctions are drawn between them in the context of the use.
Tachyarrhythmias are episodes of high rate cardiac depolarizations, typically occurring in one chamber of the heart but which may be propagated from one chamber to the other, that are sufficiently high in rate and chaotic that cardiac output from the chamber(s) is compromised, leading to loss of consciousness and death, in the case of ventricular fibrillation or weakness and dizziness in the case of atrial fibrillation or flutter and non-sinus atrial and ventricular tachycardias. Atrial fibrillation and flutter is debilitating but not life threatening unless it leads to ventricular fibrillation.
Fibrillation has generally been treated by means of high energy defibrillation shocks or pulses, which, in the context of implantable anti-arrhythmia devices, are applied by means of large surface area electrodes, including an electrode on or in the chamber to be defibrillated. The high energy level is employed in order to simultaneously depolarize the bulk of the heart chamber to be defibrillated, which will include tissues in all stages of the depolarization-repolarization cycle at the time the pulse is delivered.
Atrial fibrillation is probably the most common cardiac arrhythmia as reported in The Framingham Study reported in "Epidemiologic Features of Chronic Atrial Fibrillation", THE NEW ENGLAND JOURNAL OF MEDICINE, 306:17 1018-22, 1992, by W. Kannel, M.D. et al. Atrial fibrillation results in twice as many hospitalizations annually as bradycardia or ventricular tachyarrhythmia. The Framingham Study found an overall incidence of atrial fibrillation of approximately 0.1% per year among adults ages 25-64 years, and the prevalence in this population was approximately 2%.
Atrial fibrillation is associated with strokes thought to be caused by blood clots forming in areas of stagnant blood flow as a result of prolonging atrial fibrillation. In addition, patients afflicted with atrial fibrillation generally experience palpitations of the heart and may even experience dizziness or even loss of consciousness. Atrial fibrillation is otherwise not inherently life threatening if the ventricles are beating normally, but presumably may precipitate a life threatening ventricular tachyarrhythmia.
Atrial fibrillation occurs suddenly and many times can only be corrected by a discharge of electrical energy to the heart through the skin of the patient by way of an external defibrillator of the type well known in the art. Care must be taken in delivering the atrial cardioversion shock outside the vulnerable period of the ventricles. This treatment is commonly referred to as synchronized cardioversion and, as its name implies, involves applying electrical defibrillating energy to the heart in synchronism with a detected ventricular electrical activation (R-wave) of the heart outside of the vulnerable period. The treatment is very painful and, unfortunately, most often only results in temporary relief for patients, lasting but a few weeks.
Drugs are available for reducing the incidence of atrial fibrillation. However, these drugs have many side effects and many patients are resistant to them which greatly reduces their therapeutic effect.
Automatic implantable atrial defibrillators have been proposed to provide patients suffering from occurrence of atrial fibrillation with relief. For example, improved implantable atrial defibrillator and lead systems are described in the above-referenced '769 application and in commonly assigned U.S. Pat. Nos. 5,165,403, 5,292,338, and 5,314,430 incorporated herein by reference in their entireties. Delivery of an atrial defibrillation pulse at an inappropriate time in the cardiac cycle may induce ventricular arrhythmias, including ventricular fibrillation. An atrial sense amplifier and fibrillation detector is included in these systems to determine when the atria of the heart are in need of cardioversion, and a ventricular sense amplifier is included for sensing the R-waves. The atrial fibrillation detector causes a cardioverter stage to deliver defibrillating or cardioverting electrical energy to the atria in timed relation to a detected R-wave of the heart to avoid delivering the atrial cardioversion pulse into the vulnerable period of the ventricles.
In the system described in the '338 patent, for example, the output signal of the ventricular sense amplifier is also analyzed by a ventricular fibrillation detector to recognize ventricular fibrillation or other life threatening tachyarrhythmias. In the event that ventricular fibrillation or another life threatening ventricular arrhythmia is induced or occurs spontaneously, a ventricular cardioversion therapy is delivered to the ventricles. As a result, the atria can be automatically and safely cardioverted.
Unfortunately, the quantity of electrical energy which is required to cardiovert or defibrillate the atria is sufficient, in most cases, to cause a sudden, propagated pain in the patient's chest area or to stun the patient. Typically reported defibrillation thresholds between transvenous lead beating electrodes placed to provide atrial cardioversion pathways between the right atrium (RA) and coronary sinus (CS) or the superior vena cava (SVC) and CS are 1.3.+-.0.4 J. Significant discomfort and often intolerable pain is associated with transvenous shock therapy in this range, resulting in the need for sedation of some patients and refusal to accept the therapy by other patients.
In addition, the successful cardioversion or defibrillation of the atria may also result in a rapid decrease in the patient's heart rate from a high and possibly variable heart rate. This rapid change in heart rate can, for some patients, cause discomfort or even temporary dizziness.
The atrial defibrillator and method of U.S. Pat. No. 5,332,400 provides a warning to the patient that an atrial cardioversion shock is about to be delivered in the form of electrical energy applied to internal tissue of the patient and being of a quantity so as to be discernable by the patient without pain or other undesirable effects. The warning also provides a sufficient time in advance of the delivery of the cardioverting shock to afford the patient with an opportunity to prepare for it. For example, if the patient is standing or walking and receives the warning, the patient may wish to find a place to sit in preparation. As another example, if the patient is driving an automobile and receives the warning, the patient may wish to safely pull off the road and park in preparation.
In summary, implantable atrial cardioverters capable of generating electrical energy of sufficient amplitude and duration delivered via either epicardial or endocardial electrodes have proven effective in converting atrial fibrillation or tachycardia to normal sinus rhythm. However, with delivered shock energy exceeding 1.0 joule, intractable pain occurs to the conscious patient which drastically limits the utility of this therapy, especially if atrial cardioversion is required several times a day.
Ventricular cardioversion shocks delivered by automatic implantable cardioverter/defibrillators are typically an order of magnitude greater in energy, in the range of 10.0-30.0 joules. However, the patient is usually unconscious by the time that the shock is delivered due to the loss of cardiac output. Nevertheless, patients report lingering chest muscle pain and discomfort from the successful cardioversion shock after awakening. Considerable research effort has gone into reducing the required ventricular cardioversion shock energy level in order to reduce the size and increase the longevity of the implanted device. To date, the reduced energy delivered is still great enough to result in considerable pain if the patient is still awake, and significant lingering pain exists following cardioversion shock energy delivery.
Turning to pain control through electrical stimulation, temporary or permanently implanted medical electrical nerve or spinal cord stimulation (SCS) devices for producing pain relief are widely available. The Medtronic.RTM. Itrel II implantable neurostimulation system is widely implanted for treatment and alleviation of intractable pain. Clinical reports and studies have shown that spinal cord stimulation, a.k.a. dorsal cord stimulation, appears to suppress angina pectoris pain symptoms. The effects of SCS on angina symptoms induced by pacing the subject's heart at an elevated rate been studied, as described, for example, in "Effects of spinal cord stimulation in angina pectoris induced by pacing and possible mechanism of action", BMJ, 307(21):477-450, Aug., 1993, by C. Mannheimer, MD, et al. Similar pain suppression effects have been reported in patients suffering exercise induced, or pain or fright response, angina symptoms in "Spinal cord stimulation in angina pectoris with normal coronary arteriograms", Coronary Artery Disease, 1993: 4:819-827 by T. Eliasson, MD, et al. It is postulated therein that spinal cord stimulation relieves pain by inhibiting impulse transmission in small fiber afferents by the activation of the large fiber afferents on the spinal segmental level.
Chronic angina symptoms arise at an exercise induced elevated heart rate when cardiac muscle is deprived of oxygen due to restricted arterial blood flow and lactate accumulates in the cardiac muscle deprived of oxygen. Typically, the patient reduces exercise level to lower the heart rate or is medicated. Acute angina symptoms arise in a "heart attack" when a restricted cardiac artery is blocked. Interventional therapies are required to restore the blood flow before the insufficiency results in myocardial ischemia. Neither chronic nor acute angina symptoms are necessarily related to an arrhythmia of a heart chamber which requires cardioversion and/or drug therapies to alleviate, and the SCS pain suppression described in these articles is not related to cardioversion.
Other approaches have also been proposed and nerve stimulation systems implanted in patients to control chronic angina and/or reduce a tachyarrhythmia heart rate to a normal rate. One such early implantable peripheral nerve stimulator, the Medtronic.RTM. Angistat carotid sinus nerve stimulator, operated by regulation of the patient's blood pressure through electrical stimulation of the carotid sinus nerve to initiate a reflex vagal activity which in turn effected a slowing in a patient's supraventricular tachycardia.
Electrical stimulation of the left or right vagus nerve to directly achieve this result was also implemented in the Medtronic.RTM. Barostat vagal nerve stimulator. In U.S. Pat. No. 5,330,515, a programmable, implantable vagal stimulator is described for stimulating afferent fibers for activating a descending anti-nociceptive pathway and thereby blocking incoming pain signals is described. A history of these stimulation systems and comparison to other pain control stimulation systems for various pain sources appears in the '515 patent.
The delivery of compensatory bradycardia pacing, if necessary to restore adequate cardia output, and other aspects of a combined nerve stimulator and pacemaker are described in U.S. Pat. No. 5,330,507. In U.S. Pat. No. 5,203,326, a combined antiarrhythmia pacemaker and nerve stimulator for stimulating selected autonomic nerves or ganglia in the patient's autonomic nervous system is also described. The above-referenced '278 patent application discloses a device which provides pulse bursts to the atrium, synchronized to detected atrial depolarizations, to stimulate the SA nodal fat pad and reduce the sinus rate of patients who suffer from angina. Systems of these types are not intended to cardiovert the heart nor do they have the effect of reducing pain attendant to the delivery of a defibrillation shock.
The alleviation of pain through the operation of implantable drug dispensers for automatically periodically delivering a bolus of a pain alleviating drug at a site in the body are also well known in the art. The Medtronic.RTM. SynchroMed" programmable implantable drug pump is implanted with a drug dispensing catheter for dispensing pain relieving or analgesic agent, e.g. analgesics, anesthetics, or spinal opiates, or for dispensing chemotherapy drugs or other agents to a specific body site. A combined catheter for delivering a pain relieving or analgesic agent and electrical lead for delivering electrical stimulation for treating various neurological disorders by simultaneous or sequential administration of either therapy is described, for example, in U.S. Pat. No. 5,119,832. Such a combined lead and drug dispensing catheter is currently employed in the Medtronic.RTM. Verify" temporary screening system for determining the most efficacious therapy at a given delivery site.
Returning to the treatment of atrial and ventricular tachyarrhythmias, a number of systems have been proposed to combine the delivery of an appropriate antiarrhythmic drug therapy as an alternative or companion therapy with the delivery of an appropriate cardioversion therapy as described, for example, in U.S. Pat. Nos. 4,987,897, 5,087,243 and 5,269,301. In these systems, an implantable drug delivery system is combined with an implantable pacemaker/cardioverter/defibrillator, the system having a decision making control algorithm to govern the diagnosis of the arrhythmia, prioritize the therapies to be delivered, and deliver the therapies. It is hoped that the drug therapies can reduce the frequency of the need to deliver a defibrillation shock by either suppressing the tachyarrhythmia entirely or converting it to a lower rate or less chaotic tachyarrhythmia amenable to conversion by less aggressive high rate pacing therapies. In the event that a defibrillation shock is delivered to a conscious patient, the pain attendant to the shock is not alleviated by the delivered drug therapies. Nor does the delivery of an antiarrhythmic drug reduce the pain felt by the patient awakening from a ventricular defibrillation event.
Despite these notable improvements in implantable medical device technology, a need exists to reduce the pain and discomfort attendant to the intracardiac delivery of cardioversion shocks.